eMedicine Specialties > Physical Medicine and Rehabilitation > Spinal Cord Injury

Autonomic Dysreflexia in Spinal Cord Injury: Multimedia

Author: Denise I Campagnolo, MD, MS, Director of Multiple Sclerosis Clinical Research and Staff Physiatrist, Barrow Neurology Clinics, St Joseph's Hospital and Medical Center; Investigator for Barrow Neurology Clinics; Director, NARCOMS Project for Consortium of MS Centers
Contributor Information and Disclosures

Updated: Jul 2, 2009

Multimedia

(A) A strong sensory input (not necessarily noxio...
(Enlarge Image)
Media file 1: (A) A strong sensory input (not necessarily noxious) is carried into the spinal cord via intact peripheral nerves. The most common origins are bladder and bowel. (B) This strong sensory input travels up the spinal cord and evokes a massive reflex sympathetic surge from the thoracolumbar sympathetic nerves, causing widespread vasoconstriction, most significantly in the subdiaphragmatic (or splanchnic) vasculature. Thus, peripheral arterial hypertension occurs. (C) The brain detects this hypertensive crisis through intact baroreceptors in the neck delivered to the brain through cranial nerves IX and X (Vagus). (D) The brain attempts 2 maneuvers to halt the progression of this hypertensive crisis. First, the brain attempts to shut down the sympathetic surge by sending descending inhibitory impulses. These impulses do not get to most sympathetic outflow levels because of the spinal cord injury at T6 or above. Inhibitory impulses are blocked in the injured spinal cord. In the second maneuver, the brain attempts to bring down peripheral blood pressure by slowing the heart rate through an intact vagus (parasympathetic) nerve; however, this compensatory bradycardia is inadequate and hypertension continues. In summary, the sympathetics prevail below the level of neurologic injury, and the parasympathetic nerves prevail above the level of injury. Once the inciting stimulus is removed, reflex hypertension resolves.
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(A) A strong sensory input (not necessarily noxio...

(A) A strong sensory input (not necessarily noxious) is carried into the spinal cord via intact peripheral nerves. The most common origins are bladder and bowel. (B) This strong sensory input travels up the spinal cord and evokes a massive reflex sympathetic surge from the thoracolumbar sympathetic nerves, causing widespread vasoconstriction, most significantly in the subdiaphragmatic (or splanchnic) vasculature. Thus, peripheral arterial hypertension occurs. (C) The brain detects this hypertensive crisis through intact baroreceptors in the neck delivered to the brain through cranial nerves IX and X (Vagus). (D) The brain attempts 2 maneuvers to halt the progression of this hypertensive crisis. First, the brain attempts to shut down the sympathetic surge by sending descending inhibitory impulses. These impulses do not get to most sympathetic outflow levels because of the spinal cord injury at T6 or above. Inhibitory impulses are blocked in the injured spinal cord. In the second maneuver, the brain attempts to bring down peripheral blood pressure by slowing the heart rate through an intact vagus (parasympathetic) nerve; however, this compensatory bradycardia is inadequate and hypertension continues. In summary, the sympathetics prevail below the level of neurologic injury, and the parasympathetic nerves prevail above the level of injury. Once the inciting stimulus is removed, reflex hypertension resolves.

More on Autonomic Dysreflexia in Spinal Cord Injury

Overview: Autonomic Dysreflexia in Spinal Cord Injury
Differential Diagnoses & Workup: Autonomic Dysreflexia in Spinal Cord Injury
Treatment & Medication: Autonomic Dysreflexia in Spinal Cord Injury
Follow-up: Autonomic Dysreflexia in Spinal Cord Injury
Multimedia: Autonomic Dysreflexia in Spinal Cord Injury
References
Further Reading
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References

  1. Brown R, Burton A, Macefield VG. Input-output relationships of a somatosympathetic reflex in human spinal injury. Clin Auton Res. Apr 18 2009;[Medline].

  2. Cameron AA, Smith GM, Randall DC, et al. Genetic manipulation of intraspinal plasticity after spinal cord injury alters the severity of autonomic dysreflexia. J Neurosci. Mar 15 2006;26(11):2923-32. [Medline]. [Full Text].

  3. Schottler J, Vogel L, Chafetz R, et al. Patient and caregiver knowledge of autonomic dysreflexia among youth with spinal cord injury. Spinal Cord. Mar 10 2009;[Medline].

  4. Krassioukov A, Warburton DE, Teasell R, et al. A systematic review of the management of autonomic dysreflexia after spinal cord injury. Arch Phys Med Rehabil. Apr 2009;90(4):682-95. [Medline].

  5. Tsai SJ, Ying TH, Huang YH, et al. Transperineal injection of botulinum toxin A for treatment of detrusor sphincter dyssynergia: localization with combined fluoroscopic and electromyographic guidance. Arch Phys Med Rehabil. May 2009;90(5):832-6. [Medline].

  6. McMahon D, Tutt M, Cook AM. Pharmacological management of hemodynamic complications following spinal cord injury. Orthopedics. May 2009;32(5):331. [Medline].

  7. Chen D, Apple DF Jr, Hudson LM, Bode R. Medical complications during acute rehabilitation following spinal cord injury--current experience of the Model Systems. Arch Phys Med Rehabil. Nov 1999;80(11):1397-401. [Medline].

  8. Claydon VE, Elliott SL, Sheel AW, et al. Cardiovascular responses to vibrostimulation for sperm retrieval in men with spinal cord injury. J Spinal Cord Med. 2006;29(3):207-16. [Medline]. [Full Text].

  9. Eltorai IM, Wong DH, Lacerna M, et al. Surgical aspects of autonomic dysreflexia. J Spinal Cord Med. Jul 1997;20(3):361-4. [Medline].

  10. Giannantoni A, Di Stasi SM, Scivoletto G, et al. Autonomic dysreflexia during urodynamics. Spinal Cord. Nov 1998;36(11):756-60. [Medline].

  11. Gondim FA, Lopes AC Jr, Cruz PR, et al. On the complex autonomic changes involved in the inhibition of gastrointestinal motility after spinal cord injury (SCI). Dig Dis Sci. Jun 2006;51(6):1136. [Medline].

  12. Hambly PR, Martin B. Anaesthesia for chronic spinal cord lesions. Anaesthesia. Mar 1998;53(3):273-89. [Medline].

  13. Karlsson AK. Autonomic dysreflexia. Spinal Cord. Jun 1999;37(6):383-91. [Medline].

  14. Landrum LM, Thompson GM, Blair RW. Does postsynaptic alpha 1-adrenergic receptor supersensitivity contribute to autonomic dysreflexia?. Am J Physiol. Apr 1998;274(4 Pt 2):H1090-8. [Medline]. [Full Text].

  15. Naftchi NE, Richardson JS. Autonomic dysreflexia: pharmacological management of hypertensive crises in spinal cord injured patients. J Spinal Cord Med. Jul 1997;20(3):355-60. [Medline].

  16. Pasquina PF, Houston RM, Belandres PV. Beta blockade in the treatment of autonomic dysreflexia: a case report and review. Arch Phys Med Rehabil. May 1998;79(5):582-4. [Medline].

  17. Teasell RW, Arnold JM, Krassioukov A, Delaney GA. Cardiovascular consequences of loss of supraspinal control of the sympathetic nervous system after spinal cord injury. Arch Phys Med Rehabil. Apr 2000;81(4):506-16. [Medline].

  18. Teichman JM, Barber DB, Rogenes VJ, Harris JM. Malone antegrade continence enemas for autonomic dysreflexia secondary to neurogenic bowel. J Spinal Cord Med. Jul 1998;21(3):245-7. [Medline].

  19. Vaidyanathan S, Soni BM, Sett P, et al. Pathophysiology of autonomic dysreflexia: long-term treatment with terazosin in adult and paediatric spinal cord injury patients manifesting recurrent dysreflexic episodes. Spinal Cord. Nov 1998;36(11):761-70. [Medline].

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Further Reading

Related eMedicine topics:
Athletes With Disabilities
Cardiovascular Concerns in Spinal Cord Injury
Neurogenic Bladder
Post Head Injury Autonomic Complications
Posttraumatic Syringomyelia
Spinal Cord Trauma and Related Diseases

Clinical guidelines:
Acute management of autonomic dysreflexia: individuals with spinal cord injury presenting to health-care facilities. Consortium for Spinal Cord Medicine - Private Nonprofit Organization
Paralyzed Veterans of America - Private Nonprofit Organization.  1997 Feb (updated 2001 Jul; reviewed 2006).  29 pages.  NGC:002190

Clinical trials:
Prazosin Vibrostimulation Autonomic Dysreflexia and Spinal Cord Injury Study

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Keywords

autonomic dysreflexia, dysreflexia, hyperreflexia, spinal cord injury, SCI, autonomic nervous system, sympathetic nervous system, parasympathetic nervous system, parasympathetic, spinal cord injuries, autonomic disorders, autonomic hyperreflexia, paroxysmal hypertension, hypertensive autonomic crisis, visceroautonomic stress syndrome, autonomic spasticity, sympathetic hyperreflexia, mass reflex

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Contributor Information and Disclosures

Author

Denise I Campagnolo, MD, MS, Director of Multiple Sclerosis Clinical Research and Staff Physiatrist, Barrow Neurology Clinics, St Joseph's Hospital and Medical Center; Investigator for Barrow Neurology Clinics; Director, NARCOMS Project for Consortium of MS Centers
Denise I Campagnolo, MD, MS is a member of the following medical societies: Alpha Omega Alpha, American Association of Neuromuscular and Electrodiagnostic Medicine, American Paraplegia Society, Association of Academic Physiatrists, and Consortium of Multiple Sclerosis Centers
Disclosure: Teva Neuroscience Honoraria Speaking and teaching; Serono-Pfizer Honoraria Speaking and teaching

Medical Editor

Milton J Klein, DO, MBA, Consulting Physiatrist, Heritage Valley Health System-Sewickley Hospital, Allegheny General Hospital, and Ohio Valley General Hospital.
Milton J Klein, DO, MBA is a member of the following medical societies: American Academy of Disability Evaluating Physicians, American Academy of Medical Acupuncture, American Academy of Osteopathy, American Academy of Physical Medicine and Rehabilitation, American Medical Association, American Osteopathic Association, American Osteopathic College of Physical Medicine and Rehabilitation, American Pain Society, and Pennsylvania Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Kat Kolaski, MD, Assistant Professor, Departments of Orthopedic Surgery and Pediatrics, Wake Forest University School of Medicine
Kat Kolaski, MD is a member of the following medical societies: American Academy for Cerebral Palsy and Developmental Medicine and American Academy of Physical Medicine and Rehabilitation
Disclosure: Nothing to disclose.

CME Editor

Kelly L Allen, MD, Regional Medical Director, IMX-Medical Management Services
Disclosure: Nothing to disclose.

Chief Editor

Robert H Meier III, MD, Director, Amputee Services of America; Active Medical Staff, Presbyterian/St Luke's Hospital, Spalding Rehabilitation Hospital, Select Specialty Hospital; Consulting Staff, Kindred Hospital
Robert H Meier III, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation and Association of Academic Physiatrists
Disclosure: Nothing to disclose.

 
 
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